This project will determine the anatomical substrate within the lumbosacral spinal cord which allows sparing of function to occur in the hindquarters or rats given a mid-thoracic spinal transection between birth and 12 days of age. Similar recovery does not occur after spinal transection in older rats. We will test whether sparing of function is temporally related to the formation and maturation of synapses from descending nerve tracts using electron microscopy including serial sectioning and either the anterograde diffusion of horseradish peroxidase (HRP) or the anterograde transport of 3H amino acids and autoradiography to label specific axons and synaptic endings (Experiment 1). We will also determine whether sparing of function is related to spared, regenerated, or neogenic axons which pass through the zone of transection. The techniques to be used in this experiment will include electron microscopy of the lesion site or light microscopic autoradiography after injecting the sensori-motor cortex or the L6 segment of the spinal cord to label descending corticospinal tract axons and several ascending nerve tracts which normally pass through the zone of injury (Experiment 2). Finally, we will test whether sparing of function is related to a synaptic reorganization of dorsal root, ascending, or intrinsic connections within the lumbosacral spinal cord that occurs after injury. Quantitative comparisons will be made in animals spinally transected or hemisected at different ages. The techniques used to label specific types of axons and synaptic endings in this experiment will include the anterograde diffusion of HRP, the Fink-Heimer degeneration method, and the anterograde transport of 3H amino acids and autoradiography. The synaptic development of intrinsic connections will be studied using a morphometric electron microscopic analysis (Experiment 3).